[Weightlessness and astronautics. Current trends in physiological research].
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Biomedical subjects
Publications and source records attributed to D Lagneaux.
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Consequences of hypoxic hypobaric chemostimulation have been analyzed in six normal subjects arriving in excellent ambient conditions in a mountain scientific station (Jungfraujoch, 3,580 m). During the first two days of the sojourn, neither systemic blood pressure, nor catecholamines urinary excretion were modified in comparison with their values at the sea level. It is concluded that the chemostimulation due to hypobaric hypoxia does not affect orthosympathetic activities as far as other stressing solicitations are avoided (muscular exercise, temperature modifications, psychic alertness...etc.).
A computerized method for the measurement of alveolar ventilation (VA) and the mean alveolar partial pressures of CO2 and O2 is described and tested in healthy, awake fullterm (FT) newborns and preterm (PT) infants (postnatal age 40 days). This study emphasizes the technical pitfalls generally encountered when dealing with very small infants. A sensitive pneumotachograph with a small dead space volume and a low-flow sampling system for the gas analyzer are minimum requirements. Under these technical conditions, the major problem is the scanning time of the mass spectrometer (50 Hz), which fixes the time constant, as well as the digitization sampling rate of the gas signals. This rate was not sufficient when the respiratory rate was above 90 min-1. As critical visual evaluation of each breath is required, fully automatic access to mean alveolar data is not possible. The mean dead-space volume in both FT and PT infants was 2 ml.kg-1, with a VD/VT ratio of 0.3. The mean alveolar point was 2/3 VT, as found in adults. When expressed as ml.min-1.kg-1, VA appeared to be higher than in other studies, but related to the metabolic requirements. (VCO2 = 7.8 +/- 0.2 ml.min-1.kg-1 and VO2 = 8.0 +/- 0.2 ml.min-1.kg-1), in accordance with the state of vigilance of the neonates. Indeed, the PACO2 values, which depend on the ratio VCO2/VA, are in agreement with the values of PaCO2 generally considered normal in healthy newborns over 1 week of age.(ABSTRACT TRUNCATED AT 250 WORDS)
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In pentobarbitalized rats, hypoxia induced by inhalation of O2 8%-N2 92%, produces a transient hyperventilation which is followed by a respiratory depression and an apnea. A cardiovascular collapse is then observed. Correction of the hypocapnia depending on the initial hyperventilation, by inhalation of a gas mixture containing 4% CO2 maintains the hyperventilation and suppresses the cardiovascular collapse. Carbon dioxide activity is both a direct one by stimulation of respiratory centers and an indirect one by increasing the sensitivity of the peripheral arterial chemoreceptors to hypoxia. Four percent carbon dioxide just compensating hypocapnia are sufficient to prevent apnea and vascular collapse. The increase of this concentration up to hypercapnia complicates the interpretation of the results by addition of hypoxic and hypercapnic effects.
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In pentobarbital-anesthetized rats, hyperventilatory responses to rectangular mild hypercapnic normoxic gas mixtures inhalation were analysed. Hyperventilation dynamics were characterized by a logarithmic curve whose delay (T0) and half response time (T50-T0) were calculated. These values were established in nervously intact (IR), vagotomized (XT), surgically chemodenervated (CDN) rats and in IR-rats after almitrine bismesylate (ALM) pretreatment. In IR and XT-rats, T0 and T50 - T0 were larger after 0.5 and 1.0% CO2 step-changes than after 1.5% CO2 step-change (10 sec vs 2 sec for T0). In CDN rats, this 1.5% CO2 hyperventilation was delayed, but this delay was shorter (5 sec) than in IR or XT rats inhalating 0.5 and 1.0% CO2. After ALM pretreatment, the amplitude of the ventilatory response to a same rise in PETCO2 was increased. T0 and T50 - T0 during 0.5 and 1.0% CO2 step-changes became identical to the time values obtained with the 1.5% CO2 mixture in untreated rats. Variations in amplitude and dynamics of the ventilatory responses to CO2 provoked by ALM pretreatment may be explained by an increased sensitivity of the peripheral chemoreceptors to CO2, T0 at the time of the weakest stimuli becoming equal to that observed for a higher hypercapnia and no longer different from the lung to carotid bodies circulation time. So, the delayed and smoothed responses to 0.5 and 1.0% CO2 in IR and XT rats were attributed to a PaCO2 too weak to stimulate the peripheral chemoreceptors. The latency and half response time were higher than in CDN rats due to a weaker induced difference in PETCO2. Hyperventilation dynamics changes induced by ALM allowed to differentiate between peripheral and central chemoreception in ventilatory control.
As interactions between peripheral chemoreceptors stimulation (PCS) and pulmonary vasomotor tone remain controversial, experiments were made in rats in order to clear up the effects of PCS on pulmonary arterial pressure (PAP). Different stimulations varying in intensities were used, in rats nervously intact (IR-rats), after vagotomy (XT-rats), after chemodenervation obtained without vagotomy (CDN not XT-rats) or with XT (CDN + XT) and finally after alpha 1-receptors blockade (P-rats = pretreated rats). The observed variations were analysed in view of disentangling reflex part of PCS from a direct activity on the pulmonary vascular bed. Ventilation, PAP and systemic blood pressure (BP) were studied in anaesthetized rats. N2 test, NaCN test, 20 s of 5% O2 inhalation and almitrine bismesylate (ALM) were used as PCS, ranged in the order of their relative intensities, from the ventilatory responses observed in IR-rats. In IR-rats, N2-and CN test produced a similar transient increase of PAP, slightly more extended than the hyperventilation. After XT, the responses were prolonged, but amplified only in CN test. Ventilatory responses disappear after CDN, but as far as pulmonary hypertension is concerned, CDN + XT is more potent than CDN without XT to reduce or even suppress them. This fact is particularly evident with ALM who is the strongest PCS used. Similar reduction of PAP rise was also produced in P-rats in which ventilatory responses remain unchanged. Prolonged hypoxic inhalation induced a progressive fall of systolic BP and of PAP. The return to normal air breathing is followed by BP restoration and a long-lasting PAP increase.(ABSTRACT TRUNCATED AT 250 WORDS)
Free peritoneal mast-cells of the rat are stimulated in vitro by molecular oxygen as well as by hydrogen peroxide. Histamine release is also observed in vivo when molecular oxygen or diluted solutions of hydrogen peroxide are injected into the peritoneal cavity of the rat. Inflammatory lesions are produced (vascular congestion, oedema, exudate) which are suppressed by pretreatment with anti-H1 antihistaminics. When hydrogen peroxide solutions are more concentrated, inflammation is also provoked but antihistaminics are no more inhibitory. Mast-cells of the skin and of the lungs are not stimulated neither by molecular oxygen, nor by hydrogen peroxide.
In normal pentobarbitalized Wistar rats, simultaneous section of Hering nerves and resection of superior cervical sympathetic chain, suppress chemosensibility, in 50% cases: ventilatory responses to cyanide and to hypoxia are completely suppressed by the surgical denervation. Vagotomy completes loss of chemosensibility in a few animals, indicating the presence of intrathoracic chemoreceptors of minor importance. Local anaesthesia with lidocaïne of extra craniobasal unidentified structures, is as effective as surgical chemodenervation for suppressing ventilatory responses. This technic is not suitable for experimental purposes in long duration assays.
In pentobarbitalized rats, exogenous dopamine inhibits ventilation by acting on peripheral chemoreceptors. This inhibition is suppressed by haloperidol and by domperidone. Almitrine bismesilate, a potent glomic stimulant, potentiates dopaminergic inhibitory responses by depletion of dopamine endogenous stores. After blockade by dopamine antagonists, as well as after dopamine depletion, ventilatory responses to NaCN i.v. is increased. This potentiation can be explained by the suppression of a negative feed-back control dependent on endogenous dopamine release during the glomic stimulation itself.
During immersion in sitting position to the neck of 9 normal adult males, no change has been observed in the concentration of circulating ADH (1.91 +/- 0.58 versus 2.08 +/- 0.76 pg.ml-1) after 45 minutes. In the same period, diuresis is significantly increased (1.26 +/- 0.14 versus 3.9 +/- 1.19 ml.min-1).
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Normal rats exposed during one hour to pure normobaric oxygen, present pulmonary parenchymatous lesions: diffuse congestion, subpleural atelectasis in dissiminated small areas and hemorragic infarcts. Neither alveolar oedema nor abnormal vascular permeability have been observed. The lesions are not suppressed by pretreatment with promethazine (1 or 2 mg. 100 g-1).